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Use of soil adsorbent is an effective method for the promotion of phosphorus adsorption capacity of soil, though most of the soil adsorbents have weak phosphorus retention ability. Herein, we compared the traditional gypsum (GP) and zeolite (ZP) adsorbents to explore the phosphorus retention ability of lanthanum modified walnut shell biochar (La-BC) in soil. The results showed that with the increase of exogenous phosphorus concentration, the adsorption amount of phosphorus by adsorbents in soil increased at first and then tended to be stable. The maximum adsorption capacity of soil to phosphorus is gypsum, lanthanum-modified biochar > zeolite, and the addition of lanthanum-modified biochar can improve the adsorption capacity of soil to phosphorus, enhance the binding strength of soil and phosphorus, improve the ability of soil to store phosphorus, reducing phosphorus adsorption saturation, and is beneficial to control the leaching of soil phosphorus. FTIR and XRD analysis showed that the adsorption of phosphorus by each adsorbent in soil was mainly chemical precipitation. The response surface analysis showed that the adsorption performance of La-BC+S was the best when the concentration of exogenous phosphorus was 50.0 mg/L, pH was 6.47, and the reaction time was 436.98 min. This study provides a reference for soil adsorbents to hold phosphorus and reduce the risk of phosphorus leaching to avoid groundwater pollution.

Nasopharyngeal carcinoma (NPC) progression is regulated by genetic, epigenetic, and epitranscript modulation. As one of the epitranscript modifications, the role of N6-Methyladenosine (m

The correct presentation of Figure 9 has been redrawn and submitted because of the partial text deviation caused by the problem in Figure 9 itself.

Normal human embryonic stem cells (hESCs) can develop neoplastic cancer stem cell (CSC) properties after coculture with transformed hESCs in vitro. In the present study, the influence of the tumor microenvironment on malignant transformation of bone marrow stromal cells (BMSCs) was studied after allografting a mixture of enhanced green fluorescent protein (EGFP)-labeled BMSCs and C6 glioma cells into the rat brain to understand the influence of the cellular environment, especially the tumor environment, on the transformation of grafted BMSCs in the rat brain. We performed intracerebral transplantation in the rat brain using EGFP-labeled BMSCs coinjected with C6 tumor cells. After transplantation, the EGFP-labeled cells were isolated from the tumor using fluorescence-activated cell sorting, and the characteristics of the recovered cells were investigated. Glioma-specific biomarkers of the sorted cells and the biological characteristics of the tumors were analyzed. The BMSCs isolated from the cografts were transformed into glioma CSCs, as indicated by the marked expression of the glioma marker GFAP in glioma cells, and of Nestin and CD133 in neural stem cells and CSCs, as well as rapid cell growth, decreased level of the tumor suppressor gene p53, increased level of the oncogene murine double minute gene 2 (MDM2), and recapitulation of glioma tissues in the brain. These data suggest that BMSCs can be transformed into CSCs, which can be further directed toward glioma formation under certain conditions, supporting the notion that the tumor microenvironment is involved in transforming normal BMSCs into glial CSCs.

The earliest HSCs are derived from haemogenic endothelium via endothelial-to-haematopoietic transition during vertebrate embryogenesis; however, the underlying mechanism is largely unclear. Here we show that interplay of Smad1/5 and ERK signalling is essential for haemogenic endothelium-based HSC emergence. Smad1/5 directly inhibits erk expression through recruiting HDAC1 to and inducing de-acetylation of the erk promoter in endothelial cells. Over-activated ERK signalling conferred by inhibition of Smad1/5 promotes the arterial endothelial cell fate and constitutively strengthens the tight junction between endothelial cells, thereby repressing the specification of haemogenic endothelium and the following endothelial-to-haematopoietic transition process. These findings provide new insights into the in vitro generation of transplantable HSCs for potential clinical applications. Vertebrate haematopoietic stem cells are produced from the haemogenic endothelium by an endothelial-to-haematopoietic transition. Here, the authors show that, in zebrafish and mice, this transition depends on interplay of Smad transcription factors and the ERK signalling pathway.